Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet aggregation responses to 5-hydroxytryptamine (5-HT) were measured in plasma from migrainous subjects taking either methysergide maleate or ergotamine tartrate and were found to be reduced. Blood 5-HT levels of subjects free of headache were not affected by these drugs. The results support the hypothesis that methysergide and ergotamine act by occupying 5-HT uptake sites in vessel walls, leaving 5-HT molecules available to occupy receptors concerned with vasoconstriction.
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PMID:Effects of ergotamine and methysergide on blood platelet aggregation responses of migrainous subjects. 483 55

The hypothesis that migraine is caused by a primary abnormality of platelet behaviour was investigated in a total of 77 migraine patients and control subjects. Platelets taken from patients with classical migraine during a headache-free period demonstrated significantly higher spontaneous platelet aggregation and platelet adhesion than platelets from controls. Platelet 5-hydroxytryptamine release within three days of a migraine attack was significantly less than that measured during a migraine-free interval. Platelets from migraine patients differ significantly in their behaviour from normal platelets, and these differences can explain the onset and recurrence of attacks.
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PMID:Migraine: a platelet disorder. 611 59

The authors report a case involving a 65-year-old woman with DSM-III criteria for major unipolar depression in whom the administration of zimelidine, a potent and selective 5-hydroxytryptamine reuptake inhibitor, led to the development of a hypersensitivity reaction characterized by a severe headache, low grade fever, abnormal liver enzymes, and generalized myalgia 10 days after initiation of treatment. The most novel aspect of this hypersensitivity reaction to zimelidine was the development of abnormalities in muscle creatine phosphokinase in conjunction with the myalgia.
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PMID:Myalgia and elevation in muscle creatine phosphokinase during zimelidine treatment. 623 35

The human dorsal hand vein, exhausted in vivo (tachyphylaxis) by repeated inoculations of 5-hydroxytryptamine, recovers its capacity to contract in response to the 5HT when naloxone (per se ineffective) is inoculated into the same vein. It would seem, therefore, that in the 5HT tachyphylactic mechanism a role could be played by the progressive excitation of a local opioid modulator apparatus (silent in basal condition); naloxone's capacity for neutralizing the vein's fatigue could be indirect evidence of this. This postulation of an opioid role in the tachyphylactic mechanism differs from the conventional thesis, which explains tachyphylaxis as a progressive exhaustion of NA released from the sympathetic neuron by 5HT (see Table 1). Tachyphylaxis is poor, delayed or absent in migraine sufferers; this anomaly is present even in the period between attacks. The anomaly of inverted tachyphylaxis appears amplified during attacks. The loss or inversion of 5HT-tachyphylaxis is constantly observed in heroin addicts during acute abstinence. The fact that the clinical phenomena of acute heroin abstinence are comparable with those of a migraine attack could be a matter for further investigation.
Cephalalgia 1983 Sep
PMID:Is acute tolerance to 5-hydroxytryptamine opioid dependent? Its absence in migraine sufferers. 631 1

In thirty patients with common migraine the platelet concentrations of met-enkephalin immunoreactivity (ME) (76 +/- 9 pg/mg protein) were similar to those in 23 healthy volunteers (77 +/- 5), suggesting that there is no alteration in the ME pool in this biochemical compartment in migraine. Chronic treatment (4 weeks) with drugs that interfere with 5-hydroxytryptamine (5-HT) synthesis or uptake induced the expected changes in platelet 5-HT levels, i.e. a rise following administration of the 5-HT precursor 5-hydroxytryptophan (daily dose: 300-500 mg, n = 9) and a decrease after amine uptake inhibition by amitryptyline (30-75 mg, n = 7) and even more by chlorimipramine (30-50 mg, n = 9). Platelet ME concentrations rose by up to approximately 90% over the basal values after either 5-hydroxytryptophan (significantly from week 2) or amitriptyline (at week 2) and were unchanged after chlorimipramine, indicating that 5-HT and ME concentrations in platelets can vary independently. The high platelet ME levels following 5-hydroxytryptophan and amitriptyline cannot be explained at present. They might be due either to increased ME synthesis, possibly in the megakaryocyte, or to decreased utilization by platelets or both.
Cephalalgia 1984 Jun
PMID:Platelet met-enkephalin immunoreactivity and 5-hydroxytryptamine concentrations in migraine patients: effects of 5-hydroxytryptophan, amitriptyline and chlorimipramine treatment. 661 Apr 76

The active uptake of 5-hydroxytryptamine (5-HT) by platelets from migraine patients was measured and the results compared with 5-HT uptake of platelets from normal subjects. No significant differences in platelet 5-HT uptake were found between migraine patients and control subjects. A significant correlation was found between the length of time since the patients last migraine attack and Vmax (maximal rate of 5-HT transport). Patients who had a headache within five days prior to the test had significantly lower values of Vmax than patients without recent headaches. The implications and possible causes of this reduction in platelet 5-HT transport are discussed.
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PMID:Blood platelet 5-hydroxytryptamine accumulation and migraine. 693 52

The effect of various closely related analogues of 5-hydroxytryptamine were studied on the human basilar arterial and rat aortic strips in vitro. All analogues (except 5-methoxytryptamine) contracted both preparations producing maximal responses equivalent to that obtained with 5-hydroxytryptamine. Maximum responses to 5-methoxytryptamine were equivalent to and only 60% of the maximum obtained with 5-hydroxytryptamine on human basilar artery and rat aorta, respectively. The order of potency of the analogues on the human basilar artery was different from that obtained on the rat aorta. 5-methyltryptamine, N-methyltryptamine and tryptamine were equipotent on both tissues, whereas 5-hydroxytryptamine and 5-methoxytryptamine were 229 and 296 times more potent, respectively, on the human basilar artery compared to the rat aorta. Both tissues appear to be deficient in monoamine oxidase, since nialamide or iproniazid did not potentiate responses to tryptamine. It is concluded that the receptor type mediating contraction of the human basilar artery to 5-hydroxytryptamine is different from the classical smooth muscle D-receptor.
Cephalalgia 1981 Dec
PMID:Comparison of the contraction produced by various tryptamine analogues on human basilar arterial and rat aortic strips in vitro. 695 67

Isometric tension was recorded in ring preparations of human superficial temporal arteries contracted by noradrenaline (NA), 5-hydroxytryptamine (5-HT), and ergotamine. In contrast to NA and 5-HT, ergotamine induced long-lasting contractions refractive to additional stimulations and resistant to repeated wash-out. When tested against 5-HT, ergotamine acted as a non-competitive antagonist. When repeating the 5-HT stimulations (4.7 x 10(-5) M) the contractile response decreased indicating tachyphylaxis to this agent. As ergotamine revealed both a vasoconstrictive and a 5-HT-blocking activity, the beneficial effect in migraine may be by an interference during both the vasoconstrictory and vasodilatory phases.
Cephalalgia 1981 Dec
PMID:Effects of 5-hydroxytryptamine and ergotamine on human superficial temporal artery. 734 25

Levels of substance P (SP) and 5-hydroxytryptamine (5-HT) in platelets were measured in 25 patients with migraine, 31 patients with tension-type headache (TH) and 27 healthy controls. The mean concentration of SP in platelets was 355.3 pg/10(9) platelets in patients with migraine, 290.8 pg/10(9) platelets in patients with TH and 180.8 pg/10(9) platelets in the controls. The concentrations of platelet SP in the migrainous patients and in the TH patients were significantly higher than those in the controls. The mean concentration of 5-HT in platelets was 619.7 ng/10(9) platelets in patients with migraine, 579.3 ng/10(9) platelets in patients with TH and 811.9 ng/10(9) platelets in the controls. The concentration of platelet 5-HT in the patients with TH was significantly lower than that in the controls. The platelet SP/5-HT ratio in the migrainous patients and in the TH patients were significantly higher than that in the controls. There was significant negative correlation between the concentrations of platelet SP and those of platelet 5-HT. These results may support the hypothesis that SP released from the terminals of the trigeminal nerves causes migraine either through direct actions on the vessels or by releasing 5-HT from the platelets. The high levels of platelet SP in TH patients might reflect release of SP from the pain sensory system.
Headache
PMID:Platelet substance P and 5-hydroxytryptamine in migraine and tension-type headache. 750 72

Although migraine is inextricably bound up with 5-hydroxytryptamine and its many receptors, its precise mechanisms continue to elude us and there is still no clear evidence supporting either a vascular or neurogenic hypothesis unequivocally. What appears to distinguish migraine sufferers from normal subjects may be a greater gentic sensitivity to a wide variety of triggering agents--even including nitric oxide and the migraine aura, as well as those more usually recognized. Attention is drawn to a possible role for neurotrophins, such as the hyperalgesia-provoking nerve growth factor (NGF) in particular, as well as basic fibroblast growth factor (bFGF) and brain-derived neurotrophic factor (BDNF).
Cephalalgia 1995
PMID:Migraine to the year 2000. 758 20


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